AIM: Based on an extensive literature review, the functional matrix hypothesis was revisited in the
nineties by Moss. In his series of publications, interactions between epigenetic processes and cells
and their products leading to morphogenesis were considered to be responsible for ‘all cranial
development’. Completion of ‘the genome project’ provided an opportunity to examine the validity
of the ‘functional matrix theory’ through the use of microarray technology, real time RT-PCR and
knock out gene technology. Due to the enormity of the task at hand, it was decided to begin by
examining ‘condylar growth’. Bone fracture healing is a common experimental model to study
natural bone growth. Similarly, it was demonstrated that condylar growth induced by mandibular
advancement mirrored natural growth. Thus mandibular advancement offers a good model to study
condylar growth. It was, therefore, decided to carry out micro-array analysis of thousands of genes
expressed during condylar natural growth, and during growth induced by mandibular advancement.
In this way, interactions between epigenetic and genetic factors could be studied.
MATERIALS AND METHOD: Two hundred and eighty rats were divided into seven
experimental (advancement) and seven control groups. The rats were sacrificed at different time
points and total RNA was extracted for microarray and RT-PCR. The analysis was limited to genes
that showed a 2 or more fold change using ‘gene spring’ software.
RESULTS: Six hundred and twenty four genes showed a significant change between groups.
Knock out genes of five different identified genes demonstrated either absence or major impairment
of skeletal tissues, while normal growth of soft tissues was evident.
CONCLUSION: Genes play a fundamental role in modulating condylar growth. Levels of
expression of these genes are influenced by the surrounding functional matrix. Evidence is
therefore provided to warrant a renaming to 'The genetic functional matrix theory'.

The 81st Congress of European Orthodontic Society, Amsterdam, The Netherlands, 3–7 June 2005. In The European Journal of Orthodontics, 2006, v. 28 n. 2, p. e30 Abstract no.59

en_HK

dc.identifier.issn

0141-5387

-

dc.identifier.uri

http://hdl.handle.net/10722/94552

-

dc.description.abstract

AIM: Based on an extensive literature review, the functional matrix hypothesis was revisited in the
nineties by Moss. In his series of publications, interactions between epigenetic processes and cells
and their products leading to morphogenesis were considered to be responsible for ‘all cranial
development’. Completion of ‘the genome project’ provided an opportunity to examine the validity
of the ‘functional matrix theory’ through the use of microarray technology, real time RT-PCR and
knock out gene technology. Due to the enormity of the task at hand, it was decided to begin by
examining ‘condylar growth’. Bone fracture healing is a common experimental model to study
natural bone growth. Similarly, it was demonstrated that condylar growth induced by mandibular
advancement mirrored natural growth. Thus mandibular advancement offers a good model to study
condylar growth. It was, therefore, decided to carry out micro-array analysis of thousands of genes
expressed during condylar natural growth, and during growth induced by mandibular advancement.
In this way, interactions between epigenetic and genetic factors could be studied.
MATERIALS AND METHOD: Two hundred and eighty rats were divided into seven
experimental (advancement) and seven control groups. The rats were sacrificed at different time
points and total RNA was extracted for microarray and RT-PCR. The analysis was limited to genes
that showed a 2 or more fold change using ‘gene spring’ software.
RESULTS: Six hundred and twenty four genes showed a significant change between groups.
Knock out genes of five different identified genes demonstrated either absence or major impairment
of skeletal tissues, while normal growth of soft tissues was evident.
CONCLUSION: Genes play a fundamental role in modulating condylar growth. Levels of
expression of these genes are influenced by the surrounding functional matrix. Evidence is
therefore provided to warrant a renaming to 'The genetic functional matrix theory'.